Mechanistically, this protective effect was mediated by inhibition of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation and upregulation of light chain 3 (LC3)-dependent autophagy, which together reduced ROS-driven cellular damage and mitigated renal injury, highlighting FD@BSA as a promising strategy for AKI. Here, MAP1LC3A is linked to acute kidney injury.